About this item:

100 Views | 54 Downloads

Author Notes:

Mario Chiong, Advanced Center for Chronic Diseases (ACCDiS), Facultad Ciencias Químicas y Farmacéuticas Universidad de Chile, Santiago, Chile. Email: mchiong@uchile.cl

David Mondaca‐Ruff: Conceptualization (equal); Formal analysis (equal); Investigation (equal); Methodology (equal); Writing – original draft (equal); Writing – review & editing (equal). Clara Quiroga: Formal analysis (equal); Methodology (equal); Supervision (equal); Writing – review & editing (equal). Jaime Riquelme: Formal analysis (equal); Validation (equal); Visualization (equal); Writing – original draft (equal); Writing – review & editing (equal). Alejandra San Martín: Funding acquisition (equal); Methodology (equal); Resources (equal); Supervision (equal); Validation (equal); Writing – review & editing (equal). Mario Bustamante: Formal analysis (equal); Investigation (equal); Validation (equal); Visualization (equal). Sergio Lavandero: Funding acquisition (equal); Resources (equal); Supervision (equal); Validation (equal); Writing – review & editing (equal). Mario Chiong: Conceptualization (lead); Funding acquisition (equal); Project administration (equal); Resources (equal); Supervision (equal); Validation (equal); Visualization (equal); Writing – original draft (equal); Writing – review & editing (equal). Ignacio Norambuena‐Soto: Formal analysis (equal); Funding acquisition (equal); Investigation (equal); Writing – original draft (equal).

The authors confirm that there are no conflicts of interest.

Subject:

Research Funding:

This study was supported by Fondecyt 1180157 (MC), 1220392 (MC) and 11181000 (JAR), FONDAP 15130011 (SL, MC, JR) and the National Institute of Health, HL113167 and HL095070 (ASM). DMR was supported by Ph.D. fellowship (21130337) and MB and INS by postdoctoral fellowships 3160287 and 3210496 from ANID‐FONDECYT

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • Medicine, Research & Experimental
  • Research & Experimental Medicine
  • angiotensin II
  • AT1 receptor
  • autophagy
  • Bag3
  • LC3
  • ROCK

Regulation of total LC3 levels by angiotensin II in vascular smooth muscle cells

Tools:

Journal Title:

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Volume:

Volume 26, Number 5

Publisher:

, Pages 1710-1713

Type of Work:

Article | Final Publisher PDF

Abstract:

Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we studied how Ang II regulates LC3 levels in VSMCs and whether Bag3, a co-chaperone known to regulate LC3 total levels, may be involved in the effects elicited by Ang II. A7r5 cell line or rat aortic smooth muscle cell (RASMC) primary culture were stimulated with Ang II 100 nM for 24 h and LC3 I, LC3 II and Bag3 protein levels were determined by Western blot. MAP1LC3B mRNA levels were assessed by RT-qPCR. Ang II increased MAP1LC3B mRNA levels and protein levels of LC3 I, LC3 II and total LC3 (LC3 I + LC3 II). Cycloheximide, but not actinomycin D, abolished LC3 II and total LC3 increase elicited by Ang II in RASMCs. In A7r5 cells, cycloheximide prevented the Ang II-mediated increase of LC3 I and total LC3, but not LC3 II. Moreover, Ang II increased Bag3 levels, but this increase was not observed upon co-administration with either losartan 1 μM (AT1R antagonist) or Y-27632 10 μM (ROCK inhibitor). These results suggest that Ang II may regulate total LC3 content through transcriptional and translational mechanisms. Moreover, Bag3 is increased in response to Ang II by a AT1R/ROCK signalling pathway. These data provide preliminary evidence suggesting that Ang II may stimulate autophagy in VSMCs by increasing total LC3 content and LC3 processing.

Copyright information:

© 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/rdf).
Export to EndNote